多发性骨髓瘤
肝细胞生长因子
外域
医学
内科学
骨髓
C-Met公司
发病机制
内分泌学
受体
免疫学
作者
Karin Fahl Wader,Unn‐Merete Fagerli,Randi Utne Holt,Magne Börset,Anders Sundan,Anders Waage
标识
DOI:10.1111/j.1600-0609.2011.01622.x
摘要
The receptor tyrosine kinase c-Met and its ligand, hepatocyte growth factor (HGF), play key roles in tumour genesis and metastasis and contribute in multiple myeloma pathogenesis. Substantial data support that a soluble extracellular fragment of c-Met may function as a decoy receptor that downregulates the biological effects of HGF and c-Met. We examined serum levels of soluble c-Met in patients with myeloma and healthy individuals and investigated a possible relationship with clinical disease parameters and survival.The concentration of c-Met and HGF was measured by enzyme-linked immunosorbent assay in serum (n=49) and bone marrow plasma (n=16) from patients with multiple myeloma and in serum from healthy controls (n=26).The median serum concentration of soluble c-Met was 186 ng/mL (range 22-562) in patients with multiple myeloma and 189 ng/mL (range 124-397) in healthy individuals. There was a significant negative correlation between serum c-Met levels and disease stage, bone marrow plasma cell percentage and serum concentration of M-protein.We have for the first time examined the concentration of soluble c-Met in serum from patients with myeloma and found equal median levels in patients with myeloma as a group and healthy individuals. Still, serum levels of soluble c-Met correlated negatively with parameters of disease burden in patients with myeloma. We suggest that a possible role for the c-Met ectodomain as a negative regulator of HGF/c-Met activity should be examined in multiple myeloma.
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